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PubMed1986

Human liver fatty acid binding protein gene is located on chromosome 2.

The human gene for liver fatty acid binding protein was assigned to chromosome 2 using human-rodent somatic cell hybrids and Southern filter hybridization of cell hybrid DNA. The filters were hybridized to a radiolabeled cloned cDNA which covers 485 bases. Hybridization of the DNA to a human-specific 7.5-kb DNA fragment in HindIII-digested DNA was used to identify the human liver fatty acid binding protein gene. Results from two cell hybrids with chromosomal rearrangements suggest that the gene is on the short arm of chromosome 2.

Carrier Proteins↗
PubMed1999

[Fatty liver in adult celiac disease].

HISTORY AND ADMISSION FINDINGS: A 31-year-old woman was admitted because of heptomegaly and abnormal liver functions. For years she had suffered from diarrhoea but its cause had never been elucidated. She was underweight and had mild ankle edema. The liver margin was palpable at 20 cm below the midcostal margin, but the abdominal examination was otherwise unremarkable. INVESTIGATIONS: Sonography revealed a very large fatty liver. Biopsy showed fatty infiltration of nearly all the hepatocytes, without significant inflammation and fibrosis. Small-intestinal biopsy showed the typical histology of coeliac disease. Laboratory tests indicated abnormal liver function with increased transaminases, alkaline phosphatase, GPT and LDH, but no sign of inflammatory aetiology. These findings suggested that the liver changes were due to the coeliac disease. TREATMENT AND COURSE: After the patient had been put on a gluten-free diet the diarrhoea stopped and she started to gain weight. The liver function tests briefly became worse, but over the following 6 weeks normalized completely. The patient gained 5 kg in the subsequent 18 months and the liver became sonographically normal. The small-intestinal biopsy now showed merely discrete villar atrophy. CONCLUSION: Coeliac disease should be considered in any case of fatty liver of unknown cause. Strict gluten-free dietary treatment of the underlying cause can quickly lead to complete regression of the hepatic changes.

Adult↗
PubMed2003

Non-alcoholic fatty liver syndrome: a hepatic consequence of common metabolic diseases.

BACKGROUND AND AIMS: The association of liver steatosis with a number of common metabolic conditions has been suggested. The aim of the present study was to evaluate the clinical features of subjects with different severities of steatosis. METHODS: The present study was performed in 282 consecutive patients with 'bright liver' at ultrasonography and in 58 subjects without steatosis. They had no history of alcohol abuse and negative tests for the presence of hepatitis B and C virus. Patients underwent clinical examination, anthropometry, laboratory tests and routine liver ultrasonography. Steatosis was graded as absent, mild, moderate and severe. RESULTS: A progressive increase in the prevalence of obesity (P < 0.001), type 2 diabetes (P < 0.001), alanine aminotransferase (ALT) elevation (P < 0.001) and hypertriglyceridemia (P < 0.001), and a decrease of hypercholesterolemia (P < 0.05) was observed from the control group to the groups with mild, moderate and severe steatosis. More than half the subjects with liver steatosis had insulin resistance metabolic syndrome. Obesity, diabetes and hypertriglyceridemia were more common by 5.3-fold, 4.0-fold, and 6.7-fold, respectively, in subjects with severe steatosis, as compared to controls. Prevalence of obesity, diabetes and hyperlipidemia was significantly higher in subjects with fatty liver and ALT elevation. CONCLUSION: Fatty liver can be considered as the hepatic consequence of common metabolic diseases.

Alanine Transaminase↗
PubMed1987

Ultrasonography and echo-guided fine-needle biopsy in the diagnosis of focal fatty liver change.

The usefulness of ultrasound and echo-guided fine-needle biopsy (FNB) in the diagnosis of focal fatty liver change (FFLC) is stressed, on the basis of a retrospective series of 21 patients (8 of whom with a past history of primary cancer), followed-up for a mean period of 13.7 months. FFLC presented with various echographic patterns, shapes, dimensions and localizations. In 17 patients the diagnosis of FFLC was made by FNB, yielding cytologic and/or histological samples with steatotic, but also normal, hepatocytes. In another 4 patients the diagnosis was made by echographic follow-up. In all patients, clinical, hematological and echographic follow-up excluded the onset of neoplastic disease, confirming the high specificity of FNB in diagnosing FFLC. The possibility of changing appearance over time, and the inconstant correlation of FFLC with known causes of hepatic steatosis are discussed, as well as the hypothesis that the focal defect seen with ultrasound, could be an area of normal hepatic tissue in a fatty liver. The authors affirm the necessity to perform FNB on each doubtful lesion, but certainly when the patient has a history of malignancy.

Adult↗
PubMed1988

Molecular cloning and sequencing of DNA complementary to chicken liver fatty acid synthase mRNA.

The cDNA corresponding to 4.18 kilobases (kb) of the mRNA of chicken liver fatty acid synthase has been cloned and sequenced. The cDNA corresponds to the 3' end of the mRNA and consists of a 1.87-kb noncoding tail and a 2.31-kb region encoding 769 amino acids of the C terminus of the enzyme. The thioesterase at the C terminus, preceded by the acyl carrier protein, can be identified from known amino acid sequences. However, the identity of the enzymes N terminal to the acyl carrier protein could not be ascertained. The partial amino acid sequence of the chicken liver fatty acid synthase shows greater than 70% similarity with the rat mammary gland enzyme.

Amino Acid Sequence↗
PubMed2006

Alanine aminotransferase levels and fatty liver in childhood obesity: associations with insulin resistance, adiponectin, and visceral fat.

BACKGROUND: Concurrent with the rise in obesity, nonalcoholic fatty liver disease is recognized as the leading cause of serum aminotransferase elevations in obese youth. Nevertheless, the complete metabolic phenotype associated with abnormalities in biomarkers of liver injury and intrahepatic fat accumulation remains to be established. METHODS: In a multiethnic cohort of 392 obese adolescents, alanine aminotransferase (ALT) levels were related with parameters of insulin sensitivity, glucose, and lipid metabolism as well as adipocytokines and biomarkers of inflammation. A subset of 72 adolescents had determination of abdominal fat partitioning and intrahepatic fat accumulation using magnetic resonance imaging. FINDINGS: Elevated ALT (> 35 U/liter) was found in 14% of adolescents, with a predominance of male gender and white/Hispanic race/ethnicity. After adjusting for potential confounders, rising ALT was associated with reduced insulin sensitivity and glucose tolerance as well as rising free fatty acids and triglycerides. Worsening of glucose and lipid metabolism was already evident as ALT levels rose into the upper half of the normal range (18-35 U/liter). When hepatic fat fraction was assessed using fast magnetic resonance imaging, 32% of subjects had an increased hepatic fat fraction, which was associated with decreased insulin sensitivity and adiponectin, and increased triglycerides, visceral fat, and deep to superficial sc fat ratio. The prevalence of the metabolic syndrome was significantly greater in those with fatty liver. INTERPRETATION: Deterioration in glucose and lipid metabolism is associated even with modest ALT elevations. Hepatic fat accumulation in childhood obesity is strongly associated with the triad of insulin resistance, increased visceral fat, and hypoadiponectinemia. Hence, hepatic steatosis may be a core feature of the metabolic syndrome.

Adiponectin↗
PubMed2003

Current best treatment for non-alcoholic fatty liver disease.

Treatment of patients with non-alcoholic fatty liver disease (NAFLD) has typically been focused on the management of associated conditions such as obesity, diabetes mellitus and hyperlipidaemia. NAFLD associated with obesity may be resolved by weight reduction, although the benefits of weight loss have been inconsistent. Improving insulin sensitivity with lifestyle modifications or medications usually improves glucose and lipid levels in patients with diabetes and hyperlipidaemia. Improving insulin sensitivity is expected to improve the liver disease but in many diabetic/hyperlipidaemic patients with NAFLD, the appropriate control of glucose and lipid levels is not always accompanied by improvement of the liver condition. Results of pilot studies evaluating ursodeoxycholic acid, gemfibrozil, betaine, N-acetylcysteine, alphatocopherol, metformin and thiazolidinedione derivatives suggest that these medications may be of potential benefit. This article reviews the treatment modalities currently available for patients with NAFLD, including emerging data from clinical trials evaluating promising medications as well as possibilities for the future.

Antioxidants↗
PubMed1996

Early occurrence of acute fatty liver in pregnancy.

We report a case of acute fatty liver of pregnancy characterized by its early occurrence in the 26th wk of a twin pregnancy. Usually, this illness begins only late in the third trimester, although onset of disease as early as 26 wk has already been reported. The death of both fetuses also illustrates the high mortality rate and the necessity for prompt diagnosis and treatment.

Acute Disease↗
PubMed1967

Difference in hepatic metabolism of long- and medium-chain fatty acids: the role of fatty acid chain length in the production of the alcoholic fatty liver.

Replacement of dietary triglycerides containing long-chain fatty acids (LCFA) by triglycerides containing medium-chain fatty acids (MCFA) markedly reduced the capacity of alcohol to produce fatty liver in rats. After 24 days of ethanol and MCFA, the increase in hepatic triglycerides was only 3 times that of controls, whereas an 8-fold rise was observed after ethanol and LCFA. The triglyceride fatty acids that accumulated in the liver after feeding of ethanol with MCFA contained only a small percentage of the MCFA; their composition also differed strikingly from that of adipose lipids. To study the mechanism of the reduction in steatosis, we compared oxidation to CO(2) and incorporation into esterified lipids of (14)C-labeled chylomicrons or palmitate-(14)C (representing LCFA), and of octanoate-(14)C (as MCFA) in liver slices and isolated perfused livers, in the presence or absence of ethanol. Ethanol depressed the oxidation of all substrates to CO(2); MCFA, however, was much more oxidized and reciprocally much less esterified than LCFA, with a 100-fold difference in the ratio of esterified lipid-(14)C to (14)CO(2). Furthermore, in hepatic microsomal fractions incubated with alpha-glycerophosphate, octanoate was much less esterified than palmitate. This propensity of MCFA to oxidation rather than esterification represents a likely explanation for the reduction in alcoholic steatosis upon replacement of dietary LCFA by MCFA.

Animals↗
PubMed1999

[Acute fatty liver in pregnancy: treatment, prognosis, rules of management].

Acute fatty liver of pregnancy (AFLP), rare and potentially fatal disease, is considered as obstetric emergency. The perinatologist must be familiar with this complication of pregnancy because early diagnosis, prompt delivery and supportive care is the mainstay of therapy. When pregnant woman has nausea or vomiting, abdominal pain and jaundice, increased transaminase activity, coagulopathy and hypoglycemia during third trimester AFLP should be suspected. Mothers who have experienced AFLP must be informed of the possibility recurrence and undergo close surveillance in the next pregnancy.

Acute Disease↗
PubMed2006

Non-alcoholic fatty liver disease and the metabolic syndrome: effects of weight loss and a review of popular diets. Are low carbohydrate diets the answer?

Non-alcoholic fatty liver disease (NAFLD) encompasses a wide spectrum of fat-induced liver injury, ranging from relatively benign steatosis to cirrhosis and liver failure. The presence of obesity and insulin resistance is strongly associated with non-alcoholic fatty liver and confers on it a greater risk of histologically advanced disease. There is a growing concern in the medical profession as the prevalence of this disease continues to rise in parallel with the rise in obesity and the metabolic syndrome. Treatment options are limited and dietary weight loss is often advised. Low fat diets are difficult to adhere to and recent studies have shown the potential of low carbohydrate diets for weight loss and improving insulin resistance. Thus far, no study has evaluated the effect of low carbohydrate diets on NAFLD. Future studies will be required to address this question and others with regards to the nutritional adequacy and long-term side effects of these diets.

Diet↗
PubMed2002

Nonalcoholic fatty liver disease: pathogenesis and the role of antioxidants.

Nonalcoholic fatty liver disease (NAFLD) includes a wide spectrum of liver injury ranging from simple steatosis to steatohepatitis, fibrosis, and cirrhosis. Whereas simple steatosis has a benign clinical course, steatohepatitis is a recognized cause of progressive liver fibrosis and can develop into cirrhosis. NAFLD and nonalcoholic steatohepatitis (NASH) are the two most common chronic liver diseases in United States general population with a prevalence of 20% and 3%, respectively. Hepatic steatosis is frequently associated with obesity, type 2 diabetes, and hyperlipidemia with insulin resistance as a key pathogenic factor. A two-hit theory best describes the progression from simple steatosis to NASH, fibrosis, or cirrhosis. These two hits consist of the accumulation of excessive hepatic fat primarily owing to insulin resistance, and oxidative stress owing to reactive oxygen species (ROS). Mitochondria are the major cellular source of ROS in cases of NASH. Currently, treatment is focused on modifying risk factors such as obesity, diabetes mellitus, and hyperlipidemia. Antioxidants such as vitamin E, N-acetylcysteine, betaine, and others may be beneficial in the treatment of NASH.

Antioxidants↗
PubMed1996

Growth hormone and aging change rat liver fatty acid binding protein levels.

OBJECTIVE: Rat liver fatty acid binding protein (FABP) is believed relevant to understanding of homeostasis in lipid metabolism and lipid related diseases. Relatively little is known about endocrine control of FABP production. Thus, we examined endocrine effects on its hepatic content. METHODS/RESULTS: Hypophysectomy of 300-325 g males caused statistically significant drops of FABP levels averaging 62.2% and 67.0%, expressed g/liver or 100 g/body weight, 30-52 days after surgery. Cortisol administration (3.8 mg/kg, daily, 32-36 days) did not significantly alter this effect of hypophysectomy. Recombinant human growth hormone (GH, 2.0 U/kg, b.i.d, 17-20 days) greatly decreased the effect of hypophysectomy on FABP but had no effect in intact males. Supporting the control of FABP content by GH, FABP levels decreased significantly in 12-13 and 16-22 month old males, but not in growing, 4-6 or 10-11 month old males. FABP levels in 12-13.5 month old females also dropped significantly compared to 4-6 month old females. DISCUSSION: The importance of the data to metabolism, growth, and aging is discussed.

Aging↗
PubMed2007

1. Fatty liver and non-alcoholic steatohepatitis.

Although steatohepatitis can be induced by an excessive intake of alcohol, it can also arise through various other causes, in which case it is known as non-alcoholic fatty liver disease (NAFLD). NAFLD is classified into two categories:simple fatty liver with a favorable clinical outcome, and non-alcoholic steatohepatitis (NASH), which is intractable and progressive. Recently in Japan, there has been an increase in the number of individuals at risk of lifestyle-related diseases, due to increased insulin resistance and visceral fat obesity. The metabolic syndrome (MS) is associated with several risk factors for atherosclerosis, including diabetes mellitus (DM), hypertension, and hyperlipidemia. Visceral fat obesity is the prime cause of NASH in the liver, and is therefore considered to be one of the phenotypic features of MS. Furthermore, most chronic liver diseases are associated with hepatitis C virus (HCV) infection. Fatty degeneration of hepatocytes is often observed in the liver of HCV-infected individuals, and results from viral suppression of mitochondrial beta-oxidation of fatty acid. The natural outcome of HCV infection is worse in patients with lifestyle-related high insulin resistance and visceral fat obesity. In this review, we describe the recent advances in research on progressive liver diseases that are the result of fat accumulation in the liver, with special reference to MS.

Adipocytes↗
PubMed2006

The metabolic syndrome and nonalcoholic fatty liver disease.

Accumulating evidence supports an association between nonalcoholic fatty liver disease (NAFLD) and metabolic syndrome, diabetes, and obesity. The epidemiology, pathogenesis, and approach to treatment of NAFLD follow the same trends as these other metabolic disorders, and insulin resistance is the key event linking NAFLD to these diseases. The impairment in fat and glucose metabolism that ensues once insulin resistance occurs leads to similar biochemical and clinical abnormalities in patients with NAFLD. Many recent studies investigating the cellular and genetic basis of these diseases have led to a better understanding of their pathogenesis and insight into treatment and management. The most effective treatment thus far is weight loss and the use of insulin-modulating pharmacologic agents. A few additional treatment strategies include the use of lipid-lowering, antioxidants or cytoprotective agents, but there is no single therapeutic approach that is effective for managing NAFLD. Future therapies may combine drugs that target specific pathways involved in NAFLD pathogenesis.

Diabetes Mellitus, Type 2↗
PubMed2006

Non-alcoholic fatty liver disease and hepatitis C infection.

Non-alcoholic fatty liver disease (NAFLD) is now recognized as one of the most important causes of chronic liver disease in Western Countries, and is the hepatic manifestation of metabolic syndrome. The prevalence of NAFLD has increased with the global epidemic of obesity and type 2 diabetes mellitus. The pathophysiological hallmark of NAFLD is insulin resistance, associated with mediators of oxidative stress and inflammatory cytokines. Although simple steatosis by itself is generally benign, patients with histologically proven non-alcoholic steatohepatitis (NASH) can progress to cirrhosis. Hepatitis C (HCV) is another common cause of liver disease with some potential for progression to cirrhosis. Steatosis is present in almost 50% of patients infected by HCV. Hepatic steatosis in the setting of another liver disease (such as HCV) is associated liver disease progression. In particular, significant fibrosis is observed in patients with HCV whose liver biopsies show significant steatosis or superimposed NASH. This article reviews the host and viral factors potentially involved in the interaction between NAFLD and HCV. These factors include mediators of metabolic syndrome such as adipokines, inflammatory cytokines, factors associated with oxidative stress, lipid peroxidation products, as well as apoptosis and hepatic stellate cell activation with the resultant deposition of extracellular matrix. In addition to the mediators of metabolic syndrome (host factors), hepatic steatosis can be influenced by viral factors. The most important viral factor is HCV genotype 3, which has been independently associated with hepatic steatosis. Finally, superimposed NAFLD and visceral fat are associated with lower response rates to antiviral therapy in non-genotype 3 patients. Furthermore, viral clearance is associated with the resolution of hepatic steatosis in HCV genotype 3 but not other HCV genotypes. In these genotypes, hepatic steatosis and its impact on response to therapy are related to metabolic syndrome. Thus, the management of obesity and metabolic syndrome in patients with chronic hepatitis C may be important for reducing the risk of progression as well as improving the efficacy of antiviral therapy.

Fatty Liver↗
PubMedDate not supplied

Race and comorbid factors predict nonalcoholic fatty liver disease histopathology in severely obese patients.

PURPOSE: Nonalcoholic fatty liver disease (NAFLD) is a common and potentially serious form of chronic liver disease. Although NAFLD is known to be associated with obesity and some comorbid conditions, less is known about the severity of NAFLD among different racial groups. METHODS: We prospectively studied 237 consecutive morbidly obese patients presenting for bariatric surgery. All patients underwent intraoperative liver biopsy and chart review. After excluding subjects who reported alcohol use (n = 37) or who had missing biopsy data (n = 11), 189 patients were available for analysis. Clinical and laboratory associations with each of the histological components of NAFLD were assessed using multiple logistic regression analysis. RESULTS: The mean age was 43.1 years, 84% were female, and 13% were African American. It was found that 88% had steatosis, including 35% with moderate to severe steatosis (> 33% of hepatocytes involved). Of these patients, 67% had inflammation, 46% had fibrosis, and 45% met Brunt's criteria for NASH. Compared with Caucasians and after adjustment, African Americans had significantly lower odds of severe hepatic pathology, with adjusted odds ratios of 0.1 (P = .02) for the presence of moderate or severe steatosis, 0.2 for inflammation (P = .006), 0.3 for fibrosis (P = .05), and 0.2 for NASH (P = .02). In addition, participants with one or more features of the metabolic syndrome (ie, diabetes, hypertension, or dyslipidemia) or elevated aminotransferase levels had significantly higher odds of severe hepatic histopathology. CONCLUSION: Among obese patients presenting for bariatric surgery, NAFLD is more common in Caucasians, patients with features of the metabolic syndrome, and those with elevated aminotransferase levels.

Adult↗
PubMed2005

Insulin resistance in non-diabetic patients with non-alcoholic fatty liver disease: sites and mechanisms.

AIMS/HYPOTHESIS: Non-alcoholic fatty liver disease (NAFLD) has been associated with the metabolic syndrome. However, it is not clear whether insulin resistance is an independent feature of NAFLD, and it remains to be determined which of the in vivo actions of insulin are impaired in this condition. METHODS: We performed a two-step (1.5 and 6 pmol min(-1) kg(-1)) euglycaemic insulin clamp coupled with tracer infusion ([6,6-2H2]glucose and [2H5]glycerol) and indirect calorimetry in 12 non-obese, normolipidaemic, normotensive, non-diabetic patients with biopsy-proven NAFLD and six control subjects. RESULTS: In NAFLD patients, endogenous glucose production (basal and during the clamp) was normal; however, peripheral glucose disposal was markedly decreased (by 30% and 45% at the low and high insulin doses, respectively, p<0.0001) at higher plasma insulin levels (p=0.05), due to impaired glucose oxidation (p=0.003) and glycogen synthesis (p<0.001). Compared with control subjects, glycerol appearance and lipid oxidation were significantly increased in NAFLD patients in the basal state, and were suppressed by insulin to a lesser extent (p<0.05-0.001). The lag phase of the in vitro copper-catalysed peroxidation of LDL particles was significantly shorter in the patients than in the control subjects (48+/-12 vs 63+/-13 min, p<0.04). Lipid oxidation was significantly related to endogenous glucose production, glucose disposal, the degree of hepatic steatosis, and LDL oxidisability. CONCLUSIONS/INTERPRETATION: Insulin resistance appears to be an intrinsic defect in NAFLD, with the metabolic pattern observed indicating that adipose tissue is an important site.

3-Hydroxybutyric Acid↗